What is it about?

Capsaicin, the spicy compound in chili peppers, has numerous health benefits. It functions by activating the ion channel Transient Receptor Potential Vanilloid 1 (TRPV1) that is expressed by nociceptors, a subset of sensory peripheral neurons transmitting pain information to our brain. TRPV1 activation also induces nociceptors to locally release the vasodilator neuropeptide Calcitonin Gene-Related Peptide (CGRP). These mechanisms explain why spicy foods elicit both a burning sensation and redness. We now reveal a novel anti-viral function of capsaicin: by acting on immune cells residing in genital epithelia, namely Langerhans cells (LCs) and CD4+ T-cells that are the early cellular targets of human immunodeficiency virus type 1 (HIV-1) upon its sexual transmission, capsaicin prevents HIV-1 infection. Specifically, capsaicin activates TRPV1 in LCs and induces secretion of CGRP (like in nociceptors), which inhibits the transfer of HIV-1 captured by LCs to CD4+ T-cells. Capsaicin also inhibits direct infection of CD4+ T-cells with HIV-1, but in mechanisms that are CGRP-independent.

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Why is it important?

Activation of TRPV1 by capsaicin in nociceptors is followed by a long lasting refractory period with unresponsiveness to additional noxious stimuli. Based on these observations, topical formulations containing capsaicin have been developed and already approved clinically for pain relief. Our study suggests that such formulations might be re-positioned now as original and novel neuroimmune preventive measures against HIV-1.

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This page is a summary of: TRPV1 activation in human Langerhans cells and T cells inhibits mucosal HIV-1 infection via CGRP-dependent and independent mechanisms, Proceedings of the National Academy of Sciences, May 2023, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2302509120.
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